Bioinformatics analysis of SH2D4A in glioblastoma multiforme to evaluate immune features and predict prognosis.

IF 1.5 4区医学 Q4 ONCOLOGY

Translational cancer research Pub Date : 2024-08-31 Epub Date: 2024-08-23 DOI:10.21037/tcr-23-2000

Tian Yang, Chujun Li, Duo Xu, Rui Quan, Lansheng Wang, Yanhong Ren, Zhengkui Zhang, Rutong Yu

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引用次数: 0

Abstract

Background: Glioblastoma multiforme (GBM) is the most common and aggressive primary brain cancer in adults. This study aimed to obtain data on immune cell infiltration based on public datasets and to examine the prognostic significance of SH2 domain containing 4A (SH2D4A) for GBM.

Methods: SH2D4A expression in GBM was analyzed using a Tumor Immunity Estimation Resource (TIMER) 2.0 dataset, and a gene expression profile interaction analysis (GEPIA), and the results were validated by quantitative reverse transcription polymerase chain reaction (qRT-PCR). The Chinese Glioma Genome Atlas (CGGA) dataset was used to assess the effect of SH2D4A on GBM patient survival. The SH2D4A co-expression network of the LinkedOmics dataset and GeneMANIA dataset was also investigated. Least absolute shrinkage and selection operator (LASSO) regression models and a nomogram were constructed to assess the prognosis of GBM patients. A Gene Set Enrichment Analysis (GSEA) was performed using The Cancer Genome Atlas (TCGA) dataset to find functional differences. The relationship between SH2D4A expression and tumor-infiltrating immune cells was analyzed using xCELL, the Cell Type Identification by Estimating Relative Subsets of RNA Transcripts (CIBERSORT) algorithm, and the TIMER dataset.

Results: We discovered that SH2D4A expression was upregulated in GBM patients, and elevated SH2D4A expression was also substantially correlated with tumor grade. The survival curve analysis and multivariate Cox regression analysis showed that high SH2D4A expression was a significant independent predictor of poor overall survival (OS) in GBM patients. The immunoassay results suggested that altered SH2D4A expression may affect the immune infiltration of GBM tissues and thus the survival outcomes of GBM patients.

Conclusions: In addition to being a possible prognostic marker and therapeutic target for GBM, SH2D4A may also accelerate the progression of GBM.

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对多形性胶质母细胞瘤中的 SH2D4A 进行生物信息学分析，以评估免疫特征和预测预后。

背景：多形性胶质母细胞瘤（GBM多形性胶质母细胞瘤（GBM）是成人中最常见的侵袭性原发性脑癌。本研究旨在根据公共数据集获取免疫细胞浸润数据，并研究含 SH2 域的 4A（SH2D4A）对 GBM 的预后意义：利用肿瘤免疫估算资源（TIMER）2.0数据集和基因表达谱交互分析（GEPIA）分析了SH2D4A在GBM中的表达，并通过定量反转录聚合酶链反应（qRT-PCR）验证了结果。中国胶质瘤基因组图谱（CGGA）数据集用于评估SH2D4A对GBM患者生存的影响。此外，还研究了LinkedOmics数据集和GeneMANIA数据集的SH2D4A共表达网络。构建了最小绝对收缩和选择算子（LASSO）回归模型和提名图，以评估GBM患者的预后。利用癌症基因组图谱（TCGA）数据集进行了基因组富集分析（GSEA），以发现功能差异。使用xCELL、通过估算RNA转录本相对子集的细胞类型鉴定（CIBERSORT）算法和TIMER数据集分析了SH2D4A表达与肿瘤浸润免疫细胞之间的关系：结果：我们发现SH2D4A在GBM患者中表达上调，而且SH2D4A表达的升高与肿瘤分级有很大的相关性。生存曲线分析和多变量 Cox 回归分析表明，SH2D4A 高表达是 GBM 患者总生存期（OS）较差的重要独立预测因子。免疫测定结果表明，SH2D4A表达的改变可能会影响GBM组织的免疫浸润，从而影响GBM患者的生存结果：结论：SH2D4A不仅可能是GBM的预后标志物和治疗靶点，还可能加速GBM的进展。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Translational cancer research ONCOLOGY-

CiteScore

2.10

自引率

0.00%

发文量

252

期刊介绍： Translational Cancer Research (Transl Cancer Res TCR; Print ISSN: 2218-676X; Online ISSN 2219-6803; http://tcr.amegroups.com/) is an Open Access, peer-reviewed journal, indexed in Science Citation Index Expanded (SCIE). TCR publishes laboratory studies of novel therapeutic interventions as well as clinical trials which evaluate new treatment paradigms for cancer; results of novel research investigations which bridge the laboratory and clinical settings including risk assessment, cellular and molecular characterization, prevention, detection, diagnosis and treatment of human cancers with the overall goal of improving the clinical care of cancer patients. The focus of TCR is original, peer-reviewed, science-based research that successfully advances clinical medicine toward the goal of improving patients'' quality of life. The editors and an international advisory group of scientists and clinician-scientists as well as other experts will hold TCR articles to the high-quality standards. We accept Original Articles as well as Review Articles, Editorials and Brief Articles.